FvWRKY50 is an important gene that regulates both vegetative growth and reproductive growth in strawberry.

The WRKY transcription factors play important roles in plant growth and resistance, but only a few members have been identified in strawberry. Here we identified a WRKY transcription factor, FvWRKY50, in diploid strawberry which played essential roles in strawberry vegetative growth, and reproductive growth. Knocking out FvWRKY50 by genome editing accelerated flowering time and leaf senescence but delayed anthocyanin accumulation in fruit. Further analysis showed that FvWRKY50 acted as a transcriptional repressor to negatively regulate the expression of flowering- and leaf senescence-related genes, including FvFT2, FvCO, FvFT3, and FvSAUR36. Notably, FvWRKY50 directly upregulated the expression of FvCHI and FvDFR by binding their promoter under normal conditions, but at low temperature FvWRKY50 was phosphorylated by FvMAPK3 and then induced protein degradation by ubiquitination, delaying anthocyanin accumulation. In addition, the homozygous mutant of FvWRKY50 was smaller while the biallelic mutant showed normal size. These new findings provide important clues for us to further reveal the regulatory mechanisms of strawberry growth and fruit ripening.

[Research progress on inflammation and right ventricular failure].

OBJECTIVE: Right ventricular failure (RVF) is the main cause of death in patients with cardiopulmonary disease, such as pulmonary arterial hypertension (PAH), pulmonary embolism, acute respiratory distress syndrome, and right ventricular infarction. The exact cellular and molecular mechanisms underlying RVF remains unclear. Inflammation may play an important role during the development of RVF, as it does in left heart failure. Cardiac inflammation has been shown in RVF patients and animal models, which played a role in the impairment of the right ventricular contraction and in the maladaptive remodeling. Inflammation plays a dual role in the development of cardiopulmonary disease and its anti-inflammatory therapies may have double benefits for RVF patients. This review summarizes the evidence of inflammation in RVF and research progresses of inflammation in the development of RVF to provide a reference for further exploring the mechanism of inflammation in RVF.